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Variable strategies to solve risk–reward tradeoffs in carnivore communities 期刊论文
Proceedings of the National Academy of Sciences, 2021
作者:  Joel Ruprecht;  Charlotte E. Eriksson;  Tavis D. Forrester;  Derek B. Spitz;  Darren A. Clark;  Michael J. Wisdom;  Marcus Bianco;  Mary M. Rowland;  Joshua B. Smith;  Bruce K. Johnson;  Taal Levi
收藏  |  浏览/下载:43/0  |  提交时间:2021/08/30
3D genomics across the tree of life reveals condensin II as a determinant of architecture type 期刊论文
Science, 2021
作者:  Claire Hoencamp;  Olga Dudchenko;  Ahmed M. O. Elbatsh;  Sumitabha Brahmachari;  Jonne A. Raaijmakers;  Tom van Schaik;  Ángela Sedeño Cacciatore;  Vinícius G. Contessoto;  Roy G. H. P. van Heesbeen;  Bram van den Broek;  Aditya N. Mhaskar;  Hans Teunissen;  Brian Glenn St Hilaire;  David Weisz;  Arina D. Omer;  Melanie Pham;  Zane Colaric;  Zhenzhen Yang;  Suhas S. P. Rao;  Namita Mitra;  Christopher Lui;  Weijie Yao;  Ruqayya Khan;  Leonid L. Moroz;  Andrea Kohn;  Judy St. Leger;  Alexandria Mena;  Karen Holcroft;  Maria Cristina Gambetta;  Fabian Lim;  Emma Farley;  Nils Stein;  Alexander Haddad;  Daniel Chauss;  Ayse Sena Mutlu;  Meng C. Wang;  Neil D. Young;  Evin Hildebrandt;  Hans H. Cheng;  Christopher J. Knight;  Theresa L. U. Burnham;  Kevin A. Hovel;  Andrew J. Beel;  Pierre-Jean Mattei;  Roger D. Kornberg;  Wesley C. Warren;  Gregory Cary;  José Luis Gómez-Skarmeta;  Veronica Hinman;  Kerstin Lindblad-Toh;  Federica Di Palma;  Kazuhiro Maeshima;  Asha S. Multani;  Sen Pathak;  Liesl Nel-Themaat;  Richard R. Behringer;  Parwinder Kaur;  René H. Medema;  Bas van Steensel;  Elzo de Wit;  José N. Onuchic;  Michele Di Pierro;  Erez Lieberman Aiden;  Benjamin D. Rowland
收藏  |  浏览/下载:38/0  |  提交时间:2021/06/07
Daytime dynamo electrodynamics with spiral currents driven by strong winds revealed by vapor trails and sounding rocket probes 期刊论文
Geophysical Research Letters, 2020
作者:  R. Pfaff;  M. Larsen;  T. Abe;  H. Habu;  J. Clemmons;  H. Freudenreich;  D. Rowland;  T. Bullett;  M.‐;  Y. Yamamoto;  S. Watanabe;  Y. Kakinami;  T. Yokoyama;  J. Mabie;  J. Klenzing;  R. Bishop;  R. Walterscheid;  M. Yamamoto;  Y. Yamazaki;  N. Murphy;  V. Angelopoulos
收藏  |  浏览/下载:23/0  |  提交时间:2020/07/21
Representing the function and sensitivity of coastal interfaces in Earth system models 期刊论文
NATURE COMMUNICATIONS, 2020, 11 (1)
作者:  Ward, Nicholas D.;  Megonigal, J. Patrick;  Bond-Lamberty, Ben;  Bailey, Vanessa L.;  Butman, David;  Canuel, Elizabeth A.;  Diefenderfer, Heida;  Ganju, Neil K.;  Goni, Miguel A.;  Graham, Emily B.;  Hopkinson, Charles S.;  Khangaonkar, Tarang;  Langley, J. Adam;  McDowell, Nate G.;  Myers-Pigg, Allison N.;  Neumann, Rebecca B.;  Osburn, Christopher L.;  Price, Rene M.;  Rowland, Joel;  Sengupta, Aditi;  Simard, Marc;  Thornton, Peter E.;  Tzortziou, Maria;  Vargas, Rodrigo;  Weisenhorn, Pamela B.;  Windham-Myers, Lisamarie
收藏  |  浏览/下载:29/0  |  提交时间:2020/05/20
The structural basis for cohesin-CTCF-anchored loops 期刊论文
NATURE, 2020, 578 (7795) : 472-+
作者:  Li, Yan;  Haarhuis, Judith H. I.;  Sedeno Cacciatore, Angela;  Oldenkamp, Roel;  van Ruiten, Marjon S.;  Willems, Laureen;  Teunissen, Hans;  Muir, Kyle W.;  de Wit, Elzo;  Rowland, Benjamin D.;  Panne, Daniel
收藏  |  浏览/下载:22/0  |  提交时间:2020/07/03

Cohesin catalyses the folding of the genome into loops that are anchored by CTCF1. The molecular mechanism of how cohesin and CTCF structure the 3D genome has remained unclear. Here we show that a segment within the CTCF N terminus interacts with the SA2-SCC1 subunits of human cohesin. We report a crystal structure of SA2-SCC1 in complex with CTCF at a resolution of 2.7 angstrom, which reveals the molecular basis of the interaction. We demonstrate that this interaction is specifically required for CTCF-anchored loops and contributes to the positioning of cohesin at CTCF binding sites. A similar motif is present in a number of established and newly identified cohesin ligands, including the cohesin release factor WAPL(2,3). Our data suggest that CTCF enables the formation of chromatin loops by protecting cohesin against loop release. These results provide fundamental insights into the molecular mechanism that enables the dynamic regulation of chromatin folding by cohesin and CTCF.


The crystal structure of the SA2-SCC1 subunits of human cohesin in complex with CTCF reveals the molecular basis of the cohesin-CTCF interaction that enables the dynamic regulation of chromatin folding.


  
Global-scale human impact on delta morphology has led to net land area gain 期刊论文
NATURE, 2020, 577 (7791) : 514-+
作者:  Nienhuis, J. H.;  Ashton, A. D.;  Edmonds, D. A.;  Hoitink, A. J. F.;  Kettner, A. J.;  Rowland, J. C.;  Tornqvist, T. E.
收藏  |  浏览/下载:42/0  |  提交时间:2020/05/13

River deltas rank among the most economically and ecologically valuable environments on Earth. Even in the absence of sea-level rise, deltas are increasingly vulnerable to coastal hazards as declining sediment supply and climate change alter their sediment budget, affecting delta morphology and possibly leading to erosion(1-3). However, the relationship between deltaic sediment budgets, oceanographic forces of waves and tides, and delta morphology has remained poorly quantified. Here we show how the morphology of about 11,000 coastal deltas worldwide, ranging from small bayhead deltas to mega-deltas, has been affected by river damming and deforestation. We introduce a model that shows that present-day delta morphology varies across a continuum between wave (about 80 per cent), tide (around 10 per cent) and river (about 10 per cent) dominance, but that most large deltas are tide- and river-dominated. Over the past 30 years, despite sea-level rise, deltas globally have experienced a net land gain of 54 +/- 12 square kilometres per year (2 standard deviations), with the largest 1 per cent of deltas being responsible for 30 per cent of all net land area gains. Humans are a considerable driver of these net land gains-25 per cent of delta growth can be attributed to deforestation-induced increases in fluvial sediment supply. Yet for nearly 1,000 deltas, river damming(4) has resulted in a severe (more than 50 per cent) reduction in anthropogenic sediment flux, forcing a collective loss of 12 +/- 3.5 square kilometres per year (2 standard deviations) of deltaic land. Not all deltas lose land in response to river damming: deltas transitioning towards tide dominance are currently gaining land, probably through channel infilling. With expected accelerated sea-level rise(5), however, recent land gains are unlikely to be sustained throughout the twenty-first century. Understanding the redistribution of sediments by waves and tides will be critical for successfully predicting human-driven change to deltas, both locally and globally.


A global study of river deltas shows a net increase in delta area by about 54 km(2) yr(-1) over the past 30 years, in part due to deforestation-induced sediment delivery increase.


  
SPEN integrates transcriptional and epigenetic control of X-inactivation 期刊论文
NATURE, 2020, 578 (7795) : 455-+
作者:  Li, Yan;  Haarhuis, Judith H. I.;  Sedeno Cacciatore, Angela;  Oldenkamp, Roel;  van Ruiten, Marjon S.;  Willems, Laureen;  Teunissen, Hans;  Muir, Kyle W.;  de Wit, Elzo;  Rowland, Benjamin D.;  Panne, Daniel
收藏  |  浏览/下载:33/0  |  提交时间:2020/07/03

Xist represents a paradigm for the function of long non-coding RNA in epigenetic regulation, although how it mediates X-chromosome inactivation (XCI) remains largely unexplained. Several proteins that bind to Xist RNA have recently been identified, including the transcriptional repressor SPEN1-3, the loss of which has been associated with deficient XCI at multiple loci(2-6). Here we show in mice that SPEN is a key orchestrator of XCI in vivo and we elucidate its mechanism of action. We show that SPEN is essential for initiating gene silencing on the X chromosome in preimplantation mouse embryos and in embryonic stem cells. SPEN is dispensable for maintenance of XCI in neural progenitors, although it significantly decreases the expression of genes that escape XCI. We show that SPEN is immediately recruited to the X chromosome upon the upregulation of Xist, and is targeted to enhancers and promoters of active genes. SPEN rapidly disengages from chromatin upon gene silencing, suggesting that active transcription is required to tether SPEN to chromatin. We define the SPOC domain as a major effector of the gene-silencing function of SPEN, and show that tethering SPOC to Xist RNA is sufficient to mediate gene silencing. We identify the protein partners of SPOC, including NCoR/SMRT, the m(6)A RNA methylation machinery, the NuRD complex, RNA polymerase II and factors involved in the regulation of transcription initiation and elongation. We propose that SPEN acts as a molecular integrator for the initiation of XCI, bridging Xist RNA with the transcription machinery-as well as with nucleosome remodellers and histone deacetylases-at active enhancers and promoters.


The transcriptional repressor SPEN bridges the non-coding RNA Xist to transcription machinery, histone deacetylases and chromatin remodelling factors to initiate X-chromosome inactivation.


  
ATP13A2 deficiency disrupts lysosomal polyamine export 期刊论文
NATURE, 2020, 578 (7795) : 419-+
作者:  Nienhuis, J. H.;  Ashton, A. D.;  Edmonds, D. A.;  Hoitink, A. J. F.;  Kettner, A. J.;  Rowland, J. C.;  Tornqvist, T. E.
收藏  |  浏览/下载:18/0  |  提交时间:2020/07/03

ATP13A2 (PARK9) is a late endolysosomal transporter that is genetically implicated in a spectrum of neurodegenerative disorders, including Kufor-Rakeb syndrome-a parkinsonism with dementia(1)-and early-onset Parkinson'  s disease(2). ATP13A2 offers protection against genetic and environmental risk factors of Parkinson'  s disease, whereas loss of ATP13A2 compromises lysosomes(3). However, the transport function of ATP13A2 in lysosomes remains unclear. Here we establish ATP13A2 as a lysosomal polyamine exporter that shows the highest affinity for spermine among the polyamines examined. Polyamines stimulate the activity of purified ATP13A2, whereas ATP13A2 mutants that are implicated in disease are functionally impaired to a degree that correlates with the disease phenotype. ATP13A2 promotes the cellular uptake of polyamines by endocytosis and transports them into the cytosol, highlighting a role for endolysosomes in the uptake of polyamines into cells. At high concentrations polyamines induce cell toxicity, which is exacerbated by ATP13A2 loss due to lysosomal dysfunction, lysosomal rupture and cathepsin B activation. This phenotype is recapitulated in neurons and nematodes with impaired expression of ATP13A2 or its orthologues. We present defective lysosomal polyamine export as a mechanism for lysosome-dependent cell death that may be implicated in neurodegeneration, and shed light on the molecular identity of the mammalian polyamine transport system.


The lysosomal polyamine transporter ATP13A2 controls the cellular polyamine content, and impaired lysosomal polyamine export represents a lysosome-dependent cell death pathway that may be implicated in ATP13A2-associated neurodegeneration.


  
The biology of color 期刊论文
SCIENCE, 2017, 357 (6350)
作者:  Cuthill, Innes C.;  Allen, William L.;  Arbuckle, Kevin;  Caspers, Barbara;  Chaplin, George;  Hauber, Mark E.;  Hill, Geoffrey E.;  Jablonski, Nina G.;  Jiggins, Chris D.;  Kelber, Almut;  Mappes, Johanna;  Marshall, Justin;  Merrill, Richard;  Osorio, Daniel;  Prum, Richard;  Roberts, Nicholas W.;  Roulin, Alexandre;  Rowland, Hannah M.;  Sherratt, Thomas N.;  Skelhorn, John;  Speed, Michael P.;  Stevens, Martin;  Stoddard, Mary Caswell;  Stuart-Fox, Devi;  Talas, Laszlo;  Tibbetts, Elizabeth;  Caro, Tim
收藏  |  浏览/下载:48/0  |  提交时间:2019/11/27